Chapter Six. Cardiavesscular disease

Transcription

1 Chapter Six Cardiavesscular disease

2 This is the external appearance of a normal heart.the epicardial surface is smooth and glistening.the amount of epicardial fat is usual. The left anterior descending coronary artery extends down from the aortic root to the apex.

3 The aortic valve shows three thin and delicate cusps. The coronary artery orifices can be seen just above.the endocardium is smooth, beneath which can be seen a red-brown myocardium. The aorta above the valve displays a smooth intima with no atherosclerosis.

4 This is the tricuspid valve. The leaflets and thin and delicate. Just like the mitral valve, the leaflets have thin chordae tendineae that attach the leaflet margins to the papillary muscles of the ventricular wall below.

5 This is a normal coronary artery. The lumen is large, without any narrowing by atheromatous plaque. The muscular arterial wall is of normal proportion.

6 This is the normal appearance of myocardial fibers in longitudinal section. Note the central nuclei and the syncytial arrangement of the fibers, some of which have pale pink intercalated disks.

7 Atherosclerosis Arteriosclerosis : thickening and inelasticity of arteries three patterns: atherosclerosis medial calcification arteriolosclerosis

8 Atherosclerosis Characters: formation of intimal fibro fatty plaques with a central grumous core rich in lipid Atherosclerosis atheroma and sclerosis major targets: aorta and coronary and cerebral arteries account for more than half of all deaths in the Western world

9 Risk factors Four major risk factors: 1. Hyperlipidemia: hypercholesterolemia hypertriglyceridemia 2. Hypertension; 3. Smoking; 4. Diabetes mellitus.

10 Other risks: age sex: menopause familial predisposition insufficient regular physical activity competitive, stressful life style with type A personality behavior obesity

11 Hypotheses: 1. Effect of lipid; Pathogenesis 2. Endothelial cell injury; 3. Monocyte/macrophage; 4. SMC hyperplasia

12 ATHEROGENIC PROCESSES Insudation Hypothesis: Lipids in the atheroma are derived from plasma lipoproteins (LDL) in the blood. Encrustation Hypothesis: Says that small mural thrombi represent the initial event in atherosclerosis. Reaction to Injury Hypothesis: Smooth muscle cells accumulate as a response to injury, as a result of release of PDGF and other growth factors. Monoclonal Hypothesis: Points to the fact that many plaques contain cells that are mostly monoclonal. Perhaps their proliferation was due to a virus or cell-specific mutagen. Intimal Cell Mass Hypothesis: This is the initial lesion. Accumulation of smooth muscle cells at junctions and branching points of arteries. Hemodynamic Hypothesis: Atheromas tend to occur at locations of turbulence, pressure, and shear forces. Hypertension predisposes to atheromatous formation.

13 Stages of atherosclerosis From Stary HC c Lippincott and Raven years

14 1)endothelial injury: shear stress turbulent flow endothelial dysfunction increased permeability 2)lipoproteins deposit: low density lipoprotein(ldl); modified LDL; very low density lipoprotein (VLDL); 3)cellular interactions; monocytes/macrophages; smooth muscle cells; T lymphocytes

15 Types of Cholesterol Lipoproteins- 4 main classes: Chylomicrons Very low density lipoproteins (VLDL) Low Density Lipoprotein (LDL) High Density Lipoprotein (HDL)

16 Schematic structure of lipoproteins

17 Good Cholesterol vs. BAD Cholesterol HDL is known as the good cholesterol. It helps carry some of the bad cholesterol out of the body. It does not have the tendency to clog arteries. Levels should be >35 mg/dl. High levels of HDL >60 mg/dl can actually negate one other risk factor.

18 Good Cholesterol vs. BAD Cholesterol LDL is known as bad cholesterol. It has a tendency to increase risk of CHD. LDL s are a major component of the atherosclerotic plaque that clogs arteries. Levels should be <130 mg/dl.

19 Modified LDL-- oxidized LDL (1)be ingested through the scavenger receptor (2)chemotactic for circulating monocytes (3) increase monocyte adhesion (4) inhibit the motility of macrophages in lesions (5)stimulate release of growth factors and cytokines (6)cytotoxic to endothelial and smooth muscle cell (7)immunogenic

20 1. Fatty streaks: Basic pathology Grossly: soft, yellow intimal dots or streaks,( 3mm wide and up to 1.5cm long along the long axis of the vessel) Histologically: intimal aggregations of foam cells, derived from both macrophages and smooth muscle cells which ingest lipid with vacuolated cytoplasm. some cases undoubtedly regress

21 Started at young age (10-14) Develops over years in several stages myocardial infarction is sudden.

22 Early lipid depositions predicts the location of later atherosclerotic plaques Lipid deposits in a child s aorta From Davies, MJ, Woolf, N c Science Press

23 This is about as normal as an adult aorta in America gets. The faint reddish staining is from hemoglobin that leaked from RBC's following death. The surface is quite smooth, with only occasional faint small

24 Put down that jelly doughnut and look carefully at this aorta. The white arrow denotes the most prominent fatty streak in the photo, but there are other fatty streaks scattered over the aortic surface. Fatty streaks are the earliest lesions seen with atherosclerosis in arteries.

25 Foam Cells

26 2 fibrous plaques: G:1) range up to several centimeters 2) bright yellow to gray 3) raised several millimeters above the surface 4) irregular in shape M:1) small amounts of lipids; 2) fibrous cap: connective tissue cells with collagen and elastic fibers and proteoglycans

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28 3. Atheromatous plaques G: irregular in shape yellow to gray M: intimal surface: fibrous cap; center:an extracellular lipid core composed of cholesterol and cholesterol esters ( needle-like crystals); margins: lipid-laden foam cells(monocyte/smooth muscle cell derived), lymphocytes atrophy and fibrosis of the underlying media.

29 These three aortas demonstrate mild, moderate, and severe atherosclerosis from bottom to top. At the bottom, the mild atherosclerosis shows only scattered lipid plaques. The aorta in the middle shows many more larger plaques. The severe atherosclerosis in the aorta at the top shows extensive ulceration in the plaques.

30 This microscopic cross section of the aorta shows a large overlying atheroma on the left. Cholesterol clefts are numerous in this atheroma. The surface on the far left shows ulceration and hemorrhage.

31 This is a high magnification of the aortic atheroma with foam cells and cholesterol clefts.

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33 Complicated plaques: 1. Hemorrhage: balloon the plaque--rupture 2. Fissuring or ulceration :cholesterol emboli 3. Thrombosis 4. Calcification; 5. Aortic aneurysm.

34 This is coronary atherosclerosis with the complication of hemorrhage into atheromatous plaque, seen here in the center of the photograph. Such hemorrhage acutely may narrow the arterial lumen.

35 This is severe atherosclerosis of the aorta in which the atheromatous plaques have undergone ulceration along with formation of overlying mural thrombus.

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37 Seen here in a renal artery branch are cholesterol clefts of such an embolus. This patient had severe ulcerative, friable atheromatous plaques and had undergone angiography, which increases the risk for such emboli.

38 There is a severe degree of narrowing in this coronary artery. It is "complex" in that there is a large area of calcification on the lower right, which appears bluish on this H&E stain.

39 This is Monckeberg's medial calcific sclerosis, which is the most insignificant form of arteriosclerosis (both atherosclerosis and arteriolosclerosis are definitely significant).

40 As of arteries of important organ: 1. Aorta: 1)posterior wall and branch vessels of abdominal descending and thoracic aortas; 2)involved aortic valve ring-- aortic valve disease 3) less luminal narrowing and thrombosis; 4) aortic aneurysm and dissecting aneurysm. 2.coronary arteries: see later

41 Here is an example of an atherosclerotic aneurysm of the aorta in which a large "bulge" appears just above the aortic bifurcation. Such aneurysms are prone to rupture when they reach about 6 to 7 cm in size. They may be felt on physical examination as a pulsatile mass in the abdomen. Most such aneurysms are conveniently located below the renal arteries so that surgical resection can be performed with placement of a dacron graft.

42 3. Brain arteries: circle of Willis, middle cerebral artery ischemic disease brain atrophy and softening; aneurysm rupture hemorrhage

43 4. Renal arteries: nephrosclerosis 5. Arteries of upper and lower extremities: ischemia, gangrene 6. mesenteric arteries: Pain fever and so on

44 Coronary atherosclerotic heart disease (CHD) coronary heart disease (ischemic heart disease) a group of related syndromes Imbalance: myocardial oxygen demand blood supply Most due to atherosclerosis of coronary arteries

45 Cardiovascular disease claimed 39.4 percent of all deaths or 1 of every 2.5 deaths in the United States in CVD was about 60 percent of total mention mortality. This means that of over 2,400,000 deaths from all causes, CVD was listed as a primary or contributing cause on about 1,415,000 death certificates. (American Heart Disease)

46 Since 1900, CVD has been the No. 1 killer in the United States every year but Nearly 2,600 Americans die of CVD each day, an average of 1 death every 33 seconds. CVD claims more lives each year than the next 5 leading causes of death combined, which are cancer, chronic lower respiratory diseases, accidents, diabetes mellitus, influenza and pneumonia. Almost 150,000 Americans killed by CVD each year are under age 65.

47 Magnitude of the Burden Causes of Death in the United States Deaths in 1996 (thousands) 1, CVD Cancer American Heart Association Heart and Stroke Statistical Update Accidents 32.7 HIV/AIDS

48 Impact of cardiovascular disease UK men under 65 ( 42% )

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51 LAD>RCA>LCA&LCX

52 Depending on the rate and severity of coronary artery narrowing and the myocardial response: Grade I 25% Grade II 26% 50% Grade III 51% 75% GradeⅣ 76% angina pectoris myocardial infarction (MI) cardiac myosclerosis

53 The coronary extends from left to right across the middle of the picture and is surrounded by epicardial fat. Increased epicardial fat correlates with increasing total body fat. There is a lot of fat here, suggesting one risk factor for

54 This is the left coronary artery from the aortic root on the left. Extending across the middle of the picture to the right is the anterior descending branch. This coronary shows severe atherosclerosis with extensive calcification. At the far right, there is an area of significant

55 Normal and atheromatous coronary artery From Davies, MJ Atheroma Fibrous Cap sclerosis Normal coronary Atherosclerotic coronary

56 Angina pectoris Intermittent chest pain caused by reversible myocardial ischemia 1.typical (stable) Angina pectoris: chest pain associated with stress: crushing substernal sensation, radiating down the left arm. a fixed degree of atherosclerotic narrowing(75% or more)of coronary arteries the myocardial oxygen demand : basal conditions: enough increased requirements: not enough pain is relieved by rest or nitroglycerin

57 Coronary heart disease results in chest pain (angina pectoris) when lumen is focally reduced >70%. Normal coronary segment Atheroma

58 2. Variant angina: occurs at rest, awakening the patient from sleep; associated with coronary artery spasm 3.unstable Angina pectoris : preinfarction angina increased frequency; more intense and longer more serious,irreversible; acute plaque change with superimposed partial thrombosis,distal embolization of the thrombus and/ or vasospasm

59 myocardial infarction (MI) Myocardial necrosis caused by local ischemia acute MI is the most common cause of death in industrialized nations Pathogenesis: occlusion of coronary arteries preexisting AS ; artery thrombosis; vasospasm; platelet aggregation

60 The anterior surface of the heart demonstrates an opened left anterior descending coronary artery. Within the lumen of the coronary can be seen a dark red recent coronary thrombosis. The dull red color to the myocardium as seen below the glistening epicardium to the lower right of the thrombus is consistent with underlying myocardial infarction.

61 Location: the site of the occlusion and the anatomy of the coronary circulation occlusion of artery infarction of heart left anterior descending anterior and apical left ventricle coronary artery (40%-50%) anterior two thirds of the interventricular septum right coronary artery posterior wall of left ventricle (30%-40%) right ventricle posterior one third of the interventricular septum left circumflex lateral wall of the left ventricle coronary artery

62 Size: 1) subendocardial infart: no more than one second of the thickness of the ventricular wall 2) transmural infarct: most of the thickness of the ventricular wall pericardial effusion-- acute pericarditis; involve endocardium--mural thrombi

63 Morphology Appearance of MI is determined by its age: coagulation necrosis and inflammation(8-9h) formation of granulation tissue and resorption of the necrotic myocardium(7 d) organization of the granulation tissue to form a fibrous scar.(2-8w)

64 This is the left ventricular wall which has been sectioned lengthwise to reveal a large recent myocardial infarction.

65 This cross section through the heart demonstrates the left ventricle on the left.

66 The tan to white areas of myocardial scarring seen from the endocardial surface here represent a remote healed myocardial infarction.

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68 Biochemical changes: 1) glycogen loss; 2) loss of enzyme activity lactate dehydrogenase (LD) creatine kinase (CK) Troponin

69 several important complications: 1) rupture of infarct: most common between days 4 and 7 (1) rupture of the free wall of heart---massive hemopericardium- --cardiac tamponade (2) rupture of the intraventricular septum --left to right shunt (3) rupture of the infarcted papillary muscle (chordae tendineae)-- severe mitral insufficiency-left ventricular failure

70 One complication of a transmural myocardial infarction is rupture of the myocardium. This is most likely to occur in the first week between 3 to 5 days following the initial event, when the myocardium is the softest. The white arrow marks the point of rupture in this anterior-inferior myocardial infarction of the left ventricular free wall and septum. Note the dark red blood clot forming the hemopericardium. The hemopericardium can lead to tamponade.

71 In cross section, the point of rupture of the myocardium is shown with the arrow.

72 2. Ventricular aneurysms anteroapical region of the heart thin-walled, fibrous outpouching of the ventricular wall surgical resection is beneficial. 3. Mural thrombosis: endocardial surface of infarct systemic emboli and complications others: acute heart failure, cardiogenic shock 4. Acute pericarditis

73 A cross section through the heart reveals a ventricular aneurysm with a very thin wall at the arrow.

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75 Myocardial fibrosis Atherosclerosis of coronary artery --long-term ischemic myocardial injury -- myocardial atrophy,fibrosis Cardiac myosclerosis - congestive heart failure

76 Sudden coronary death Most cases are caused by heart diseases Sudden death in night. No any other lethal causes but the lesions of coronary and/or myocardium. Vasospasm of coronary

77 Treatment

78 Treatment (continued) 1) Stenting a stent is introduced into a blood vessel on a balloon catheter and advanced into the blocked area of the artery the balloon is then inflated and causes the stent to expand until it fits the inner wall of the vessel, conforming to contours as needed the balloon is then deflated and drawn back The stent stays in place permanently, holding the vessel open and improving the flow of blood.

79 Treatment (continued) 2) Angioplasty a balloon catheter is passed through the guiding catheter to the area near the narrowing. A guide wire inside the balloon catheter is then advanced through the artery until the tip is beyond the narrowing. the angioplasty catheter is moved over the guide wire until the balloon is within the narrowed segment. balloon is inflated, compressing the plaque against the artery wall once plaque has been compressed and the artery has been sufficiently opened, the balloon catheter will be deflated and removed.

80 Treatment (continued) 3) Bypass surgery healthy blood vessel is removed from leg, arm or chest blood vessel is used to create new blood flow path in your heart the bypass graft enables blood to reach your heart by flowing around (bypassing) the blocked portion of the diseased artery. The increased blood flow reduces angina and the risk of heart attack.

81 Get regular medical checkups. Control your blood pressure. Check your cholesterol. Don t smoke. Exercise regularly. Maintain a healthy weight. Eat a heart-healthy diet. Manage stress.

82 Hypertension normal blood pressure: systolic blood pressure (SBP) 18.4kPa(140mmHg) and diastolic blood pressure (DBP) 12kPa(90mmHg) the prevalence increases with age condition of patient: SBP 18.4kPa(140mmHg) and/or DBP 12kPa( 90mmHg)

83 Essential (primary ) hypertension : idiopathic hypertension 90%-95% secondary ( symptomatic) hypertension : 5%10% secondary to another disease such as renal disease narrowing of the renal arteries;adrenal disorders, primary aldosteronism, Cushing s syndrome

84 Etiology and pathogenesis: normal regulation of blood pressure 1.cardiac output blood volume heart rate left ventricular factors 2.total peripheral resistance resistance arterioles thickness of the arteriolar wall the effect of neural and hormonal influences constrict or dilate vessels

85 Hypotheses 1.neural disorder stress disorder of the central regulation of BP constrictors dilators peripheral resistance increasing 2. Endocrine disorder

86 3. Renal hypotheses renin- -angiotensin---aldosterone system juxtaglomerular cells renin ACE angiotensinogen angiotensin angiotensin2 direct action on vessel smooth muscle vasoconstriction increases distal tubular reabsorption of sodium and water

87 4.Inheritable hypotheses familial aggregation of hypertension depend on the cumulative effects of allelic forms of several genes that affect BP 5.others environmental factors obesity, smoking, heavy consumption of salt

88 Complex disorder more than one cause disturbances in any of the factors genetically predisposed individual

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90 Type and pathology 1. benign hypertension remaining at a modest level; fairly stable over years to decades; with long life. 1. Functional change of vessels (first stage) arterial discontinuous spasm; BP change; no obviously clinical feature.

91 2.structure changes of vessels 1). hyaline arteriole arterial continuous spasm--increased permeability of the small vessels-endothelial injury--plasma proteins deposition microscopically vessel wall replaced by homogenous eosinophilic material ; Reduction of luminal diameter.

92 2). muscular arteries progressive thickening of their walls hypertrophy of the muscular media and later fibrosis; fibroelastic hyperplasia high increasing BP; obviously clinical features.

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94 3.organ changes ( third stage ) 1)heart : hypertensive heart disease compensation : concentric left ventricular hypertrophy grossly : large size, heavy weight, thickened wall and papillary muscles microscopically : hypertrophy myocardium enlarge nuclei decompensation : ventricular dilatation cardiac failure(left right)

95 The left ventricle is markedly thickened in this patient with severe hypertension that was untreated for many years. The myocardial fibers have undergone hypertrophy.

96 This left ventricle is very thickened, but the rest of the heart is not greatly enlarged. This is typical for hypertensive heart disease. The hypertension creates a greater pressure load on the heart to induce the hypertrophy.

97 2) kidney :hypertensive nephrosclerosis grossly: small and hard with a surface of diffuse, fine granularity; cut surface : atrophic thinning of the cortex; poor demarcation of cortex from medulla.

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99 Hyaline arteriolosclerosis is seen in the elderly, but more advanced lesions are seen in persons with diabetes mellitus and/or with hypertension.

100 microscopically: hyaline arteriolosclerosis: hyaline thickening of the walls of the small arteries and arterioles--narrowed lumen-decreased blood flow---ischemic atrophy nephron: some atrophy some hypertrophy interstitial fibrosis and lymphocytic infiltrate clinical feature: proteinuria

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102 3)brain cerebral edema increaseinintracranial pressure herniation softeningof thebrain cerebral hemorrhages most complication, mostlocations basal nucleus;internal capsule

103 Hemorrhages involving the basal ganglia area (the putamen in particular) tend to be non-traumatic and caused by hypertension, which damages and weakens the small penetrating arteries.

104 The large hemorrhage in this adult brain arose in the basal ganglia region of a patient with hypertension. This is one cause for a "stroke".

105 4)retinal changes Grade1 silver wiring of the arteries Grade3 retinal hemorrhages and exudations, papilloedema; visual impairments

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107 Malignant hypertension 1. Far less common, young people; 2. Charactristic change fibrinoid necrosis of arterioles and arteries; hyperplastic arterioles;an onion-skin appearance 3. Rapidly rising BP especially DBP 130mmHg

108 4. necrotizing glomerulitis with micro thrombi proteinuria,hematuria,azotemia, uremia; obvious retinal changes retinal hemorrhages and exudates, papilloedema, visual impairments,blindness 5. Most patients die of uremia, cerebral hemorrhage and cardiac failure within1-2 years without treatment.

109 The second form of arteriolosclerosis is shown here. The arteriole here has an "onion skin" appearance typical of hyperplastic arteriolosclerosis. This lesion is most often associated with malignant hypertension.

110 One complication of hyperplastic arteriolosclerosis with malignant hypertension is fibrinoid necrosis, as seen here in a renal arteriole.

111 Rheumatism introduction Concept Rheumatic fever is an acute, immunologically mediated, multisystem inflammatory diseases. That follows, after a few weeks, an episode of group A streptococcol pharyngitis.

112 Etiology and pathogenesis induced by group A, b-hemolytic streptococci Evidence: 1. the onset of symptoms 2 to 3 weeks after infection and the absence of streptococci 2. High anti streptolysin o (ASO) titer 3. Declined remarkably over the past 30 years because of the rapid diagnosis and treatment of streptococcol pharyngitis

113 4. Non suppurative disease no streptococci can be found directly in lesions. Immunologically mediated streptococci antistreptococci M-protein antibodies C-antigen(glycoprotein) tissue (joints) cross reactions to myocardium to connective

114 Pathogenesis and key morphologic changes of acute rheumatic heart disease.

115 basic pathology basic lesions: fibrinoid necrosis Aschoff bodies three stages : 1. Alteration and exudation; 1 month mucoid change fibrinoid necrosis cellular infiltration lymphocytes, monocytes plasma cells etc.

116 2. Proliferation or granuloma. (last 2-3 months) characteristic lesion Aschoff body, rheumatic granuloma location : interstitial connective tissue of myocardium, especially near small blood vessels. Under endocardium and skin. shape : round or spindle

117 composition : central focus :fibriniod necrosis surrounded by : chronic inflammatory cells and characteristic histiocytes : anitschkow cells Aschoff cells :large histiocytes, multinucleated, vesicular abundant basophilic cytoplasm cross-section : owls eyes cells; longitudinal section : caterpillars cells.

118 Microscopically, acute rheumatic carditis is marked by a peculiar form of granulomatous inflammation with so-called "Aschoff nodules" seen best in myocardium.

119 Here is an Aschoff nodule at high magnification. The most characteristic component is the Aschoff giant cell. Scattered inflammatory cells accompany them and can be mononuclears or occasionally neutrophils.

120 Another peculiar cell seen with acute rheumatic carditis is the Anitschkow myocyte. This is a long, thin cell with an elongated nucleus.

121 Aschoff cell

122 Aschoff body in the heart

123 3. Healing or fibrous scar fibroblast cells collagen scar all stages last 4-6 months

124 3 Fibrous scar formation (2-3 months)

125 Rheumatic heart disease Rheumatic pancarditis : 1. Rheumatic endocarditis 2. Rheumatic myocarditis 3. Rheumatic pericarditis

126 rheumatic endocarditis location: common ; affect any valves 1 mitral valves alone, 70-75; 2 mitral and aortic valves, 25 3 other valves

127 lesions: 1. edematous and thickened valves; 2. formation of small, grey vegetations along the lines of valve closure-verrucous endocarditis M: 1. foci of fibrinoid necrosis, but Aschoff bodies are not common 2. vegetations consist of fibrin and platelets

128 Acute rheumatic mitral valvulitis superimposed on chronic rheumatic heart disease. Small vegetations are visible along the line of closure of the mitral valve leaflet (arrows).

129 Chronic rheumatic myocarditis. The mitral valve leaflets are thickened, opaque and fused at the commissures. The chordae tendineae are also thickened and shortened as a result of fibrosis.

130 In time, chronic rheumatic valvulitis may develop by organization of the acute endocardial inflammation along with fibrosis, as shown here affecting the mitral valve. Note the shortened and thickened chordae tendineae.

131 Prognosis 1.the acute changes may resolve without severe scarring and chronic valvalar deformities. 2. The repeat lesions make the valves fibrous thicken and adherent, chordae tendineae thicken and shorten.

132 Mac callum s plaque lesions organization thickened and rough endocardium especially in the posterior wall of left atrium thrombosis

133 Rheumatic myocarditis stromal connective tissue; edema, fibrinoid necrosis, Aschoff bodies, scar. Sometime, the myocardium may also contain diffuse interstitial edema and inflammatory infiltrates, these cause cardiac failure especially happen in children.

134 Rheumatic pericarditis fibrinous pericarditis cor villosum: organization, adhesion constrictive pericarditis

135 The epicardial surface of the heart shows a shaggy fibrinous exudate. This is another example of fibrinous pericarditis. The fibrin often results in the the finding on physical examination of a "friction rub" as the strands of fibrin on epicardium and pericardium rub against each other.

136 Acute fibrinous pericarditis. The normally smooth, glistening pericardial surface is covered by shaggy fibrinous exudate. In this case, the pericarditis developed because of uremia and caused a fatal cardiac tamponade.

137 Changes of other organs (1) Rheumatic arthritis 1.large joints: wrists, elbows, ankles, knees; 2.migratory polyarthritis; 3.stiffness, swelling, pain 4.chronic inflammatory infiltrates and edema sometime Aschoff bodies in the involved joints and periarticular soft; 5.self-limited,do not cause chronic deformity.

138 (2) Rheumatic arteritis coronary, renal, mesenteric and cerebral arteries as well as aortic and pulmonary vessels. Wall of vessels : edema, fibrinoid necrosis, inflammatory cells infiltration, Aschoff bodies, fibrious scar.

139 (3) skin change exudation lesion: erythema marginatum proliferation lesion: subcutaneous nodules (4) rheumatic lesion of central nerve system 5-12 children rheumatic arteritis neuron cells change proliferation of microglia cells chorea minor

140 Rheumatic pneumonitis and pleuritis are uncommon interstitial inflammatory infiltrates fibrous inflammation of the pleural surface hyaline membrane

141 Infective endocarditis infection of the cardiac valves or surface of endocardium any type of microorganisms, fungus, virus, most cases are caused by bacteria

142 Acute bacteria Subacute high virulence low virulence staphylococcus aureus a-hemolytic streptococci infective focal suppuration septicemia focal inflammatory -bacteremia way endocarditis septicemia endocarditis last time acute, severe, short long, more than 6 weeks no more than 6 weeks valve normal, healthy valve damaged valves especially mitral valve such rheumatic endocarditis lesions suppuration necrosis tissue chronic changes ulcer, rupture thicken, shallow ulcer granulation tissue vegetations single or multiple vegetations similar as acute large, grey-yellow and friable endocarditis platelets+ fibrin(thrombus) platelets+ fibrin(thrombus) necrosis tissue +bacterium necrosis tissue +bacterium + neutrophilic leucocytoes inflammatory cells

143 Acute clinical features 1.high fever,chills Subacute 1.Low fever, malaise weight loss 2. Blood cultures(-) 3.system embolic 2. Blood cultures (+) 3. multiple abscesses ( often develop at the sites of infarcts ) prognosis 1. Acute valve insufficiency 1.chronic valve diseases rupture of the leaflets, 2.Embolism infarct in the chordae tendineae brain, kidney, myocardium. 2. chronic valve diseases 3. embolism septice infarction, multiple abscesses

144 There are irregular vegetation attached to the valve, which has been severely damaged and perforated. The metal probe is traversing a hole in the valve leaflet.

145 Acute bacterial endocarditis of the aortic valve. Opened right atrium shows large, irregular, friable vegetations causing virtual occlusion of the tricuspid valve.

146 Irregular reddish tan vegetations overlie valve cusps that are being destroyed. Portions of the vegetation can break off and become septic emboli.

147 Microscopically, the valve in infective endocarditis demonstrates friable vegetations of fibrin and platelets (pink) mixed with inflammatory cells and bacterial colonies (blue).

148 Here is a valve with infective endocarditis. The blue bacterial colonies on the lower left are extending into the pink connective tissue of the valve. Valves are relatively avascular, so high dose antibiotic therapy is needed to eradicate the infection.

149 This is infective endocarditis. The aortic valve demonstrates a large, irregular, reddish tan vegetation.

150 The rheumatic fever phase of RHD (rheumatic heart disease) is marked by a row of small, warty vegetations along the lines of closure of the valve leaflets. IE (infective endocarditis) is characterized by large, irregular masses on the valve cusps that can extend onto the chordae. NBTE (nonbacterial thrombotic endocarditis) typically exhibits small, bland vegetations, usually attached at the line of closure. One or many may be present. LSE (Libman-Sacks endocarditis) has small or medium-sized vegetations on either or both sides of the valve leaflets.

151 Valvular disease congenital and acquired valvulitis irreversible deformity of valves Stenosis and Insufficiency increase pressure load and volume load hemodynamic changes cardiac failure

152 normal blood flow way: tricuspid valve pulmonary valve blood of systematic veins right artrium right ventricle pulmonary arteries lung mitral valve aortic valve lung pulmonary veins left artrium left ventricle aorta systematic arteries

153 Lung Vena cava Right artrium Right ventricle systematic arteries Pulmonary veins Left artrium Pulmonary arteries Left ventricle Aorta

154 1. Mitral stenosis: normal area of mitral orifice : 5cm2 narrow to a slit like channel, designated fish mouth deformity 1. Dilated and hypertrophied left atrium 2. Chronic passive congestion of lung: firm and heavy lung 3. Pulmonary hypertension: dilated and hypertrophied right ventricle 4. Dilated and hypertrophied right atrium: systematic congestions

155 The heart has been sectioned to reveal the mitral valve as seen from above in the left atrium. The mitral valve demonstrates the typical "fish mouth" shape with chronic rheumatic scarring.

156 Seen from the left atrial side, the mitral valve appears markedly stenotic, appearing as a pinhole (arrow).

157 Lung Vena cava Right artrium Right ventricle systematic arteries Pulmonary veins Left artrium Pulmonary arteries Left ventricle Aorta

158 2. Mitral insufficiency 1. Dilated and hypertrophied left heart 2. Chronic passive congestion of lung 3. Pulmonary hypertension ; dilated and hypertrophied right ventricle 4. Dilated and hypertrophied right atrium ;systematic congestions main difference : dilated and hypertrophied left ventricle

159 Lung Vena cava Right artrium Right ventricle systematic arteries Pulmonary veins Left artrium Pulmonary arteries Left ventricle Aorta

160 3. Aortic stenosis compensation concentric hypertrophy decompensation dilation of chamber

161 Degeneration calcific aortic stenosis. View from the aortic side of an unopened, markedly deformed tricuspid aortic valvle. Calcific masses protrude into the sinuses of Valsalva.

162 In contrast, healed rheumatic aortic valvalitis shows aortic stenosis due to fibrosis and fusion of the valves and the commissures.

163 Lung Vena cava Right artrium Right ventricle systematic arteries Pulmonary veins Left artrium Pulmonary arteries Left ventricle Aorta

164 4. Aortic insufficiency hypertrophy of left ventricle left heart failure passive congestion of lung Pulmonary hyper tension right heart failure systematic congestions

165 Lung Vena cava Right artrium Right ventricle systematic arteries Pulmonary veins Left artrium Pulmonary arteries Left ventricle Aorta

166 心瓣膜病 二尖瓣 狭窄 心形 梨形心 左房肥大 杂音 舒 隆 临床 关闭不全 主A瓣 狭窄 球形心 靴形心 左心肥大 左室肥大 全心肥大 收 吹 收 吹 左心衰 右心衰 关闭不全 靴形心 左室肥大 舒 吹